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Nervous System > Infections in the CNS > Flashcards

Infections in the CNS Flashcards

1
Q

define meningitis

A

infection/inflammation of the meninges

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2
Q

define encephalitis

A

infection/inflammation of the brain substance

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3
Q

define myelitis

A

inflammation/infection of the spinal cord

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4
Q

what is the classical triad of meningitis?

A

> fever
neck stiffness
altered mental status

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5
Q

what are the clinical features of meningitis?

A 
> short history of progressive headache
> petechial skin rash (non-blanching)
> cranial nerve palsy
> seizures
> focal neurological deficit
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6
Q

what is the differential diagnosis for meningitis?

A

> infective: bacterial, viral and fungal
inflammatory: sarcoidosis
drug induced: NSAIDs, IVIG
malignant: metastatic, haematological

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7
Q

what are the bacterial causes of meningitis?

A

> Neisseria meningitidis : meningococcus

> streptococcus pneumonia : pneumococcus

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8
Q

what are the viral causes of meningitis?

A

enteroviruses

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9
Q

what are the clinical features of encephalitis?

A 
> flu like prodrome
> progressive headache with associated fever
> progressive cerebral dysfunction
> seizures
> focal symptoms/signs
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10
Q

what is the difference between viral encephalitis and bacterial meningitis?

A

viral encephalitis is generally slower and cerebral dysfunction is a more prominent feature

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11
Q

what is the differential diagnosis for encephalitis?

A 
> infective: viral
> inflammatory: limbic encephalitis
> metabolic: hepatic, uraemic, hyperglycaemic
> malignant: metastatic, paraneoplastic
> migraine
> post ictal
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12
Q

what are the two antibodies involved in autoimmune encephalitis?

A

> anti-VGKC (voltage gated potassium channel)

> anti-NMDA receptor

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13
Q

describe the clinical features of Anti-VGKC encephalitis

A

> frequent seizures
amnesia (not able to retain new memories)
altered mental state

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14
Q

describe the clinical features of anti-NMDA receptor

A

> flue like prodrome
prominent psychiatric features
altered mental state and seizures
progressing to a movement disorder and coma

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15
Q

what investigations would you carry out for meningitis?

A

> blood cultures
lumbar puncture
there is no need to image if there are no contraindications to lumbar puncture

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16
Q

what investigations would you carry out for encephalitis?

A

> blood cultures
CT (+/- MRI)
lumbar puncture
EEG

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17
Q

what are the contraindications for a lumbar puncture?

A

> focal symptoms or signs suggesting a focal brain mass
reduced conscious level suggesting raised intracranial pressure
in the immunocompromised you should image first as some features can be lost

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18
Q

what CSF findings would you find in bacterial meningitis?

A

> increased opening pressure
high neutrophillic cell count
reduced glucose (as bacteria consume glucose)
high protein

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19
Q

describe the CSF findings in viral meningitis and encephalitis

A

> normal/increased opening pressure
high mainly lymphocytic cell count
normal glucose
slightly increased protein

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20
Q

what is the commonest cause on encephalitis in Europe?

A

herpes simplex encephalitis

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21
Q

what is the lab diagnosis for herpes simplex encephalitis?

A

PCR of CSF for viral DNA

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22
Q

how do you treat herpes simplex encephalitis?

A

aciclovir in clinical suspicion

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23
Q

where does the herpes simplex virus remain latent?

A

in the trigeminal ganglion or sacral ganglion

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24
Q

how are enterovirses spread?

A

by the faecal-oral route

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25
Q

what can cause non-paralytic meningitis?

A

enteroviruses

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26
Q

do enteroviruses causes gastroenteritis?

A

no

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27
Q

how are arbovirus encephalitides transmitted?

A

by vector (mosquito or tick) from non-human host

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28
Q

give some examples of arbovirus encephalitides?

A

> west nile virus
st louis encephalitis
western equine encephalitis
Japanese b encephalitis

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29
Q

define a brain abscess

A

localised area of pus within the brain

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30
Q

what is a subdural empyema?

A

thin layer of pus between the dura and arachnoid membrane over the surface of the brain

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31
Q

what are the clinical features of brain abscesses and empyema?

A 
> fever
> headache
> focal symptoms and signs (depressed conscious level)
> meningism (particularly in empyema)
> features of the underlying source
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32
Q

name some causes of brain abscesses and empyema

A

> penetrating head injury
spread form adjacent infection (dental, sinusitis, otitis media)
blood borne infection
neurosurgical procedure

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33
Q

how would you diagnose a brain abscess and empyema?

A

> imaging: CT or MRI
investigate source
blood cultures
biopsy (drainage of pus)

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34
Q

what streptococci group are often present in brain abscesses?

A

penicillin sensitive strep-milleri group (strep. anginosus, strep intermedius, strep constellatus)

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35
Q

in a brain abscess is there more likely to be one organism present of a mixture of organisms present?

A

a mixture of organisms

36
Q

how would you manage a brain abscess?

A

> surgical drainage if possible

> high dose antibiotics (culture and sensitivity tests on aspirate provide useful guide)

37
Q

what antibiotics could you give to cover strep infection in a brain abscess?

A

> penicillin

> ceftriaxone

38
Q

what treatment would you give for an anaerobic brain abscess?

A

metronidazole

39
Q

name HIV indicator illnesses

A 
> cerebral toxoplasmosis
> aseptic meningitis/encephalitis
> primary cerebral lymphoma
> cerebral abscess
> cryptococcal meningitis
> space occupying lesion of unknown cause
> dementia
> leucoencephalopathy
40
Q

what brain infections could you see in HIV patients with low CD4 counts?

A 
> Cryptococcus neoformans
> toxoplasma gondii
> progressive multifocal leukoencephalopathy
> crytomegalovirus
> HIV encephalopathy
41
Q

what tests could you carry out to differentiate the causative organisms in HIV low CD4 count brain infections?

A 
> india ink, cryptococcal antigen
> toxoplasmosis serology
> JC virus PCR
> CMV PCR
> HIV PCR
42
Q

what do cryptococcal antigens loos like in an indian ink stain?

A

as a capsule organism in double circles

43
Q

what spirochaetes infections involve the CNS?

A

> lyme disease
syphilis
leptospirosis

44
Q

how is lyme disease transmitted?

A

vector borne, tick

45
Q

describe stage one in lyme disease?

A

> early localised infection
erythema migrans: characteristic expanding rash at site of tick bite
50% flue like symptoms

46
Q

describe stage 2 lyme disease

A

> early disseminated infection (weeks-months)
one or more organ system involvement
musculoskeletal and neurological involvement

47
Q

what neurological involvement is there in stage 2 lyme disease if the patient is untreated?

A 
> mononeuropathy
> mononeuritis multiplex
> painful radiculoneuropathy
> cranial neuropathy
> myelitis
> meningo-encephalitis
48
Q

describe stage 3 lyme disease

A

> chronic infection occurring after a period of latency

> musculoskeletal and neurological involvement is the most common

49
Q

what are the investigations for lyme disease?

A 
> serological tests
> CSF lymphocytosis
> PCR of CSF
> MRI brain/spine
> nerve condition studies
50
Q

what is the treatment for lyme disease?

A

> intravenous ceftriaxone

> oral doxycycline

51
Q

when does tertiary syphilis (neurosyphilis)occur?

A

years/decades after primary disease

52
Q

what tests are carried out for neurosyphilis?

A

> treponema specific antibody test
non-treponemal specific antibody test
CSF PCR

53
Q

how does the CSF change in neurosyphilis?

A

> CSF lymphocytes increase

> there is evidence of intrathecal antibody production

54
Q

what is the treatment for neurosyphilis?

A

high dose penicillin

55
Q

what causes poliomyelitis?

A

poliovirus type 1,2 or 3 (enterovirus)

56
Q

what part of the central nervous system does paralytic poliomyelitis affect?

A

the anterior horns of the lower motor neurons

57
Q

describe the paralysis seen in poliomyelitis

A

> asymmetric
flaccid paralysis
no sensory features

58
Q

in the uk what polio types does the vaccine contain?

A

all three types

59
Q

rabies is described as neurotropic. what does this mean?

A

the virus enters the peripheral nerves and migrates to CNS

60
Q

what is there at the site of the initial lesion in rabies?

A

paraesthesiae

61
Q

what is the affect of rabies infection?

A

> ascending paralysis

> encephalitis

62
Q

how would you diagnose rabies encephalitis?

A

> culture (detection or serology)

63
Q

who is given the rabies pre-exposure prevention?

A

> bat handlers
regular handlers of imported animals
selected travellers to enzootic areas

64
Q

what is the rabies post exposure treatment?

A

> wash wound
active rabies immunisation
human rabies immunoglobulin (passive immunisation) if high risk

65
Q

what is the bacteria involved in tetanus infection?

A

clostridium tetani:
anaerobic gram positive bacillus
spore forming

66
Q

describe the pathology of tetanus

A

toxin acts on the neuro-muscular junction blocking inhibition of motor neurons causing rigidity or spasm

67
Q

describe the prevention of tetanus

A

> immunisation (toxoid) combined with other antigens

> penicillin and immunoglobulin for high risk wounds/patients

68
Q

describe the bacteria involved in botulism

A

clostridium botulinum

> anaerobic spore producing gram positive bacillus

69
Q

describe the effect of the neurotoxin in botulism

A

> binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
toxin binding blocks acetylcholine release

70
Q

what is the recovery form botulism neurotoxin?

A

sprouting new axons

71
Q

where is clostridium botulism naturally present?

A

> soil
dust
aquatic environments

72
Q

what are the three modes of infection of botulism?

A

> infantile (intestinal colonisation)
food-borne
wound (drug abuse)

73
Q

what is the clinical presentation of botulism?

A 
> incubation period (4-14 days)
> descending symmetrical flaccid paralysis
> pure motor
> respiratory failure
> autonomic dysfunction
74
Q

how do you diagnose botulism?

A

> nerve conducting studies
mouse neutralisation bioassay for toxin in blood
culture from debrided wound

75
Q

what is the treatment for botulism?

A

> anti-toxin
penicillin/metronidazole
radical would debridement

76
Q

name a post infective inflammatory syndrome affecting the central nervous system

A

acute disseminated encephalomyelitis

77
Q

name a post infective inflammatory syndrome affecting the peripheral nervous system

A

guillain barre syndrome

78
Q

what is the aetiology of Creutzfeldt-Jakob disease?

A

> sporadic
new variant
familial
acquired (cadaveric growth hormone, dura matter grafts, blood transfusion)

79
Q

what should you consider in any rapidly progressing dementia?

A

sporadic CJD

80
Q

what are the clinical features of sporadic CJD?

A 
> insidious onset
> early behavioural abnormalities
> rapidly progressing dementia
> myoclonus
> progressing global neurological decline
> motor abnormalities
> cortical blindness
> seizures (sometimes)
81
Q

what is the differential diagnosis for sporadic CJD?

A

> Alzheimer’s disease my myoclonus
subacute sclerosing panencephalitis
CNS vasculitis
inflammatory encephalopathies

82
Q

what is the prognosis of sporadic CJD?

A

> rapid progression

> death within 6 months

83
Q

what is new variant CJD linked to?

A

bovine spongiform encephalopathy in cattle

84
Q

what is the difference in the clinical features of new variant CJD compared to sporadic CJD?

A

> early behavioural changes are more important

> longer course (average 13 months)

85
Q

what is the investigation for Creutzfeldt-Jakob disease?

A

> MRI (pulvinar signs in variant)
EEG (generalised periodic complexes typical though often normal)
CSF (normal or raised protein. immunoassay 14-3-3-brain protein)

Nervous System (45 decks)

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